“…Although the thalamocortical input to the neocortex is purely excitatory (glutamatergic), as determined by electrophysiological, electron microscopic, and immunocytochemical evidence (White, 1978;Ferster and Lindstrom, 1983;Agmon and Connors, 1992;Kharazia and Weinberg, 1993), inhibitory (GABAergic) mechanisms are recruited from the very first stage of intracortical processing. Indeed, electrical stimulation of thalamocortical afferents in vivo (Ferster and Lindstrom, 1983;Swadlow, 1989Swadlow, , 1990 or in vitro (Agmon and Connors, 1992;Gil and Amitai, 1996), as well as controlled sensory stimulation (Simons and Carvell, 1989;Simons, 1995;Brumberg et al, 1996;Swadlow et al, 1998;Zhu and Connors, 1999), result in a brief excitation of neocortical neurons, immediately followed by a pronounced inhibitory response mediated by intracortical inhibitory interneurons. The short latency of the inhibitory response indicates that the inhibitory interneurons eliciting it must be excited directly by the thalamocortical afferents, consistent with anatomical data (White, 1978;FairĂ©n and Valverde, 1979;Freund et al, 1985;Keller and White, 1987), and in turn inhibit other cortical neurons disynaptically.…”